2. Academic Validation
  3. An ethanolic extract of Arctium lappa L. leaves ameliorates experimental atherosclerosis by modulating lipid metabolism and inflammatory responses through PI3K/Akt and NF-κB singnaling pathways

An ethanolic extract of Arctium lappa L. leaves ameliorates experimental atherosclerosis by modulating lipid metabolism and inflammatory responses through PI3K/Akt and NF-κB singnaling pathways

  • J Ethnopharmacol. 2024 Jan 20:117768. doi: 10.1016/j.jep.2024.117768.
Hui Guo 1,  Bing-di Cui 2,  Man Gong 3,  Qing-Xia Li 4,  Ling-Xia Zhang 5,  Jia-Li Chen 6,  Jun Chi 7,  Li-Li Zhu 8,  Er-Ping Xu 9,  Zhi-Min Wang 10,  Li-Ping Dai 11
Affiliations

Affiliations

  • 1 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: guohui2008no.1@163.com.
  • 2 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: 1628639250@qq.com.
  • 3 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: man.gong_2019@hactcm.edu.cn.
  • 4 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: QingxiaLi0302@163.com.
  • 5 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: zhanglingxia1205@126.com.
  • 6 Department of Food Science and Engineering, Institute of Food Safety and Nutrition, Jinan University, Guangzhou, 510632, China. Electronic address: kellychan123@126.com.
  • 7 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: chijun16@126.com.
  • 8 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: zhulili911027@163.com.
  • 9 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: xuerping@sina.com.
  • 10 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China; Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China. Electronic address: zhmw123@163.com.
  • 11 Henan University of Chinese Medicine (HUCM), Collaborative Innovation Center of Research and Development on the Whole Industry Chain of Yu-Yao, Henan Province, Zhengzhou, 450046, China. Electronic address: liping_dai@hactcm.edu.cn.
PMID: 38253275 DOI: 10.1016/j.jep.2024.117768
Abstract

Ethnopharmacological relevance: Atherosclerosis (AS), a lipid-induced inflammatory condition of the arteries, is a primary contributor to atherosclerotic cardiovascular diseases including stroke. Arctium lappa L. leaf (ALL), an edible and medicinal herb in China, has been documented and commonly used for treating stroke since the ancient times. However, the elucidations on its anti-AS effects and molecular mechanism remain insufficient.

Aim of the study: To investigate the AS-ameliorating effects and the underlying mechanism of action of an ethanolic extract of leaves of Arctium lappa L. (ALLE).

Materials and methods: ALLE was reflux extracted using with 70% ethanol. An HPLC method was established to monitor the quality of ALLE. High fat diet (HFD) and vitamin D3-induced experimental AS in rats were used to determine the in vivo effects; and oxidized low-density lipoprotein-induced RAW264.7 macrophage foam cells were used for in vitro assays. Simvatatin was used as positive control. Biochemical assays were implemented to ascertain the secretions of lipids and pro-inflammatory mediators. Haematoxylin-eosin (H&E) and Oil red O stains were employed to assess histopathological alterations and lipid accumulation conditions, respectively. CCK-8 assays were used to measure cytotoxicity. Immunoblotting assay was conducted to measure protein levels.

Results: ALLE treatment significantly ameliorated lipid deposition and histological abnormalities of aortas and livers in AS rats; improved the imbalances of serum lipids including total Cholesterol (TC), triglyceride (TG), low-density lipoprotein Cholesterol (LDL-C) and high-density lipoprotein Cholesterol (HDL-C); notably attenuated serum concentrations of inflammation-associated cytokines/molecules including TNF-α, IL-6, IL-1β, VCAM-1, ICAM-1and MMP-9. Mechanistic studies demonstrated that ALLE suppressed the phosphorylation/activation of PI3K, Akt and NF-κB in AS rat aortas and in cultured foam cells. Additionally, the PI3K agonist 740Y-P notably reversed the in vitro inhibitory effects of ALLE on lipid deposition, productions of TC, TNF-α and IL-6, and protein levels of molecules of PI3K/Akt and NF-κB singnaling pathways.

Conclusions: ALLE ameliorates HFD- and vitamin D3-induced experimental AS by modulating lipid metabolism and inflammatory responses, and underlying mechanisms involves inhibition of the PI3K/Akt and NF-κB singnaling pathways. The findings of this study provide scientific justifications for the traditional application of ALL in managing atherosclerotic diseases.

Keywords

Arctium lappa L. leaf; Atherosclerosis; Chlorogenic acid (PubChem CID:1794427); Inflammatory response; Isochlorogenic acid A (PubChem CID:6474310); Kaempferol 3-O-Rutinoside (PubChem CID:5318767); Lipid metabolism; NF-κB; PI3K/Akt; Rutin (PubChem CID:5280805).

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